Our efforts are directed toward answering the question, how do we sleep? Our experiments involve systems which we believe to be involved in the sleep disorders known as narcolepsy and insomnia. Cats with chronically implanted electrodes will be monitored for changes in sleep behavior following brainstem lesions and changes in single-unit (neuron) firing in the brainstem and cerebellum in different sleep-waking states. Cats with brainstem lesions which eliminate the atonia of paradoxical sleep will be studied in an effort to determine the neuronal pathways involved in producing atonia in normal paradoxical sleep. We hypothesize that abnormal functioning of these pathways is a critical factor in the narcoleptic attack. The nature of ponto-geniculooccipital (PGO) spikes, which occur spontaneously in paradoxical sleep, will be studied further at the single neuronal and macropotential level. We have demonstrated that PGO spikes can be elicited by environmental stimuli and have postulated that they are a general sign of alerting. We plan to study modulation of PGO spike occurrence, and thus of alerting, by the brainstem raphe nuclei. Raphe lesions produce insomnia, and we believe that to be due to altered control of alerting mechanisms.